Transformation of NIH 3T3 fibroblasts by an activated form of p59hck

Mol Cell Biol. 1989 Jun;9(6):2724-7. doi: 10.1128/mcb.9.6.2724-2727.1989.

Abstract

Phosphorylation of a tyrosine residue near the carboxy terminus of src-family protein tyrosine kinases is believed to regulate the biological activity of these gene products. Conversion of this tyrosine in p59hck (Tyr-501) to a phenylalanine residue by using oligonucleotide-directed mutagenesis yielded a product (p59hckF501) with very potent transforming activity. Quantitative analysis by a soft-agar cloning assay revealed that p59hckF501 was more than 100-fold more effective than a closely related transforming element, p56lckF505, in colony formation. Cells bearing p59hckF501 had increased levels of protein phosphotyrosine. The ability of p59hckF501 to transform NIH 3T3 cells was abolished by a second mutation believed to destroy the ATP-binding domain.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cell Transformation, Neoplastic*
  • DNA / genetics*
  • Fibroblasts / ultrastructure
  • Lysine / genetics
  • Lysine / metabolism
  • Mice
  • Moloney murine leukemia virus / genetics
  • Moloney murine leukemia virus / physiology
  • Mutation*
  • Phenotype
  • Phosphorylation
  • Protein-Tyrosine Kinases / genetics*
  • Protein-Tyrosine Kinases / metabolism
  • Transfection
  • Tyrosine / metabolism

Substances

  • Tyrosine
  • DNA
  • Protein-Tyrosine Kinases
  • Lysine